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Background Neutrophil–lymphocyte ratio (NLR) has shown a good prognostic value in many different type of malignancies. The purpose of this study was to investigate the relationship between NLR and the outcome of critically ill patients with cancer. Methods We performed a single-institution, retrospective study of 1317 adult critically ill patients with cancer and determined the optimal cut-off for NLR by X-tile software. Propensity score matching (PSM) and inverse probabilities of treatment weighting (IPTW) were performed to control confounders. Cox proportional hazards model was used to evaluate the relationship between NLR and 28-day, 6-month and 1-year all-cause mortality. Kaplan–Meier method, subgroup analysis, and receiver operating characteristics (ROC) analysis were applied to assess the prognostic value of NLR. Results The cut‐off value for NLR was 17.6. Cox proportional hazards model demonstrated that high NLR (> 17.6) was independently associated with 28-day, 6-month and 1-year all-cause mortality with hazard ratio (HR) of 1.58 (1.29, 1.94), 1.51 (1.28, 1.77) and 1.45 (1.25, 1.69), respectively. The results were consistent with survival analyses (p < 0.001, log-rank test). The ROC analyses showed that the discrimination abilities of NLR were better than other blood-based biomarkers. Conclusion NLR is a promising prognostic indicator of survival in unselected critical ill patients with cancer (AU)

Asunto(s)

Humanos , Masculino , Femenino , Anciano , Recuento de Células , Neoplasias/mortalidad , Neoplasias/fisiopatología , Neutrófilos , Linfocitos , Pronóstico , Enfermedad Crítica , Estudios Retrospectivos , Curva ROC , Análisis de Supervivencia , Factores de Tiempo

RESUMEN

BACKGROUND: Neutrophil-lymphocyte ratio (NLR) has shown a good prognostic value in many different type of malignancies. The purpose of this study was to investigate the relationship between NLR and the outcome of critically ill patients with cancer. METHODS: We performed a single-institution, retrospective study of 1317 adult critically ill patients with cancer and determined the optimal cut-off for NLR by X-tile software. Propensity score matching (PSM) and inverse probabilities of treatment weighting (IPTW) were performed to control confounders. Cox proportional hazards model was used to evaluate the relationship between NLR and 28-day, 6-month and 1-year all-cause mortality. Kaplan-Meier method, subgroup analysis, and receiver operating characteristics (ROC) analysis were applied to assess the prognostic value of NLR. RESULTS: The cut-off value for NLR was 17.6. Cox proportional hazards model demonstrated that high NLR (> 17.6) was independently associated with 28-day, 6-month and 1-year all-cause mortality with hazard ratio (HR) of 1.58 (1.29, 1.94), 1.51 (1.28, 1.77) and 1.45 (1.25, 1.69), respectively. The results were consistent with survival analyses (p < 0.001, log-rank test). The ROC analyses showed that the discrimination abilities of NLR were better than other blood-based biomarkers. CONCLUSION: NLR is a promising prognostic indicator of survival in unselected critical ill patients with cancer.

Asunto(s)

Linfocitos/citología , Neoplasias/mortalidad , Neutrófilos/citología , Anciano , Enfermedad Crítica/mortalidad , Femenino , Humanos , Estimación de Kaplan-Meier , Recuento de Linfocitos , Masculino , Pronóstico , Puntaje de Propensión , Modelos de Riesgos Proporcionales , Curva ROC , Estudios Retrospectivos , Análisis de Supervivencia , Factores de Tiempo

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Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, "Circular RNA_LARP4 inhibits cell proliferation and invasion of nasopharyngeal carcinoma by repressing ROCK1, by J.-Y. Pan, X.-L. Bao, K. Zhu, published in Eur Rev Med Pharmacol Sci 2019; 23 (22): 9915-9922-DOI: 10.26355/eurrev_201911_19557-PMID: 31799660" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/19557.

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OBJECTIVE: Astrocytes play a key role in hypoxic brain injury. The aim of our research was to determine the effects of menaquinone-7 (MK-7), a subtype of vitamin K2 (VK2), on astrocytes during hypoxia and its potential mechanisms. MATERIALS AND METHODS: Astrocytes from the palliums of newborn Sprague Dawley rats were cultured. An astrocyte-hypoxia model was established using a hypoxia workstation. Cell Counting Kit-8 (CCK-8) and BrdU assays were used to determine the effects of MK-7 on hypoxic astrocytes. 2',7'-Dichlorodihydrofluorescein diacetate (DCFDA) or dihydroethidium (DHE) assays were conducted to detect the levels of reactive oxygen species (ROS). An ATP assay was used to measure intracellular ATP production. The levels of proinflammatory cytokines and chemokines containing interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), CC-chemokine ligand 2 (CCL2), and CXC-chemokine ligand 10 (CXCL10), as well as vitamin K-dependent protein growth arrest-specific 6 (Gas6), were determined in hypoxia-induced astrocytes, in the presence or absence of MK-7 pretreatment. Small interfering RNA (siRNA) was used to knockdown Gas6 expression to determine its role in hypoxic astrocytes pretreated with MK-7. RESULTS: Hypoxia reduced astrocyte viability and proliferation significantly; however, when pretreated with MK-7, these conditions remarkably increased. MK-7 also inhibited hypoxia-induced ROS production and enhanced ATP generation of hypoxic astrocytes. Pretreatment with MK-7 effectively reduced the expression of IL-6, TNF-α, CCL2, and CXCL10 but enhanced the expression of Gas6 in hypoxic astrocytes. Gas6 inhibition markedly attenuated the decline in MK-7-induced ROS generation and IL-6 expression, and weakened MK-7-induced cell viability and ATP production in hypoxic astrocytes. CONCLUSIONS: Our study is the first to confirm that MK-7 can protect astrocytes from hypoxia-induced cytotoxicity, possibly by inhibiting mitochondrial dysfunction and the expression of proinflammatory cytokines. Gas6 may also participate in these protective effects.

Asunto(s)

Astrocitos/efectos de los fármacos , Hipoxia de la Célula/efectos de los fármacos , Péptidos y Proteínas de Señalización Intercelular/genética , Mitocondrias/efectos de los fármacos , Vitamina K 2/análogos & derivados , Vitaminas/farmacología , Adenosina Trifosfato/metabolismo , Animales , Astrocitos/metabolismo , Proliferación Celular/efectos de los fármacos , Supervivencia Celular/efectos de los fármacos , Células Cultivadas , Mitocondrias/metabolismo , Estrés Oxidativo/efectos de los fármacos , Ratas Sprague-Dawley , Especies Reactivas de Oxígeno/metabolismo , Vitamina K 2/farmacología

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OBJECTIVE: Acute liver injury (ALI) is associated with the Kupffer cells (KCs) inflammation and hepatocytes apoptosis. Previous studies have shown that miR-640 is a valid regulator of the Low-density lipoprotein receptor-related protein 1 (LRP 1) which expressed much lower in an inflammatory condition. However, it is unclear whether MiR-640 inhibition protects against ALI by the up-regulation of LRP 1. To explore the regulated mechanism of miR-640 on acute liver injury. MATERIALS AND METHODS: We analyzed the expression of miR-640 in different times of acute injured liver tissues. Lipopolysaccharide (LPS) was employed in provoking the KCs inflammation to injure liver. We used miR-640 mimic or inhibitor to improve or resist the function of miR-640 to explore miR-640 function to ALI via the target of LRP1. RESULTS: We showed that the expression of miR-640 markedly increased in LPS-induced acute injured liver tissues. LPS promoted the progress of ALI, and the inhibition of miR-640 could reverse the injured effects of LPS. Moreover, WNT signaling pathway and LRP1 were significantly enhanced by miR-640 inhibition. CONCLUSIONS: These results suggested that miR-640 promotes KCs inflammation via restraining LRP 1 and WNT signaling pathway. But inhibiting miR-640 prevents inflammation damage and ameliorates ALI. MiR-640 inhibition may become a novel target for the therapy of ALI in the future.

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Lesión Pulmonar Aguda/metabolismo , Proteína 1 Relacionada con Receptor de Lipoproteína de Baja Densidad/metabolismo , MicroARNs/metabolismo , Lesión Pulmonar Aguda/inducido químicamente , Lesión Pulmonar Aguda/patología , Animales , Células Cultivadas , Inflamación/metabolismo , Lipopolisacáridos , Masculino , Ratones , Ratones Endogámicos C57BL , MicroARNs/genética , Vía de Señalización Wnt

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OBJECTIVE: To study the influence of micro ribonucleic acid (miR)-155 on depression-like behaviors of depression mice, and to explore the role of Wnt/b-catenin signaling pathway in behavioral regulation of depression mice. MATERIALS AND METHODS: The mouse model of depression was established via chronic unpredictable mild stress (CUMS). All mice were randomly divided into control group (n=12), model group (n=12), and fluoxetine group (n=12). The expression level of miR-155 in the hippocampus of mice in each group was detected via quantitative Polymerase Chain Reaction (qPCR). The changes in the behaviors of mice in each group were evaluated via behavioral experiments. The apoptosis level in the hippocampus of mice in each group was detected via terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining. Moreover, the content of inflammatory factors in the hippocampus of mice in each group was detected using the enzyme-linked immunosorbent assay (ELISA) kits. The expression levels of Wnt/b-catenin signaling pathway-related proteins in each group were detected via Western blotting. RESULTS: The expression level of miR-155 in the hippocampus was significantly higher in model group than that in control group (p<0.01). Meanwhile, the expression level of miR-155 was significantly lower in fluoxetine group than that in model group (p<0.01). There were no statistically significant differences in the crossing score and rearing score in the open field test among groups (p>0.05). Compared with those in control group, the immobility time in tail suspension test and forced swimming test were significantly increased (p<0.01), while the sucrose preference degree significantly declined (p<0.01) in model group. Fluoxetine could significantly reduce the immobility time in tail suspension test and forced swimming test (p<0.01) and increase the sucrose preference degree (p<0.01) in model group. The number of TUNEL-positive cells in the hippocampus of mice in model group was significantly larger than that in control group (p<0.01). Fluoxetine could effectively reduce the number of TUNEL-positive cells in the hippocampus (p<0.01). Compared with those in control group, the content of tumor necrosis factor-α (TNF-a), interleukin-1b (IL-1b), and IL-6 in the hippocampus was significantly increased (p<0.01), while the content of IL-10 was significantly decreased (p<0.01) in model group. Fluoxetine could effectively reduce the content of TNF-a, IL-1b, and IL-6 (p<0.01) and increase the content of IL-10 (p<0.01). Besides, in model group, the expression levels of dishevelled-1 (DVL-1) and b-catenin in hippocampus remarkably declined (p<0.01), while the expression levels of glycogen synthase kinase-3b (GSK-3b) and adenomatous polyposis coli (APC) were remarkably increased (p<0.01) compared with those in control group. Fluoxetine could effectively lower the expressions of GSK-3b and APC in the hippocampus (p<0.01) and increase the expressions of DVL-1 and b-catenin (p<0.01) in model group. CONCLUSIONS: MiR-155 is involved in regulating the depression-like behaviors of depression mice through promoting the release of inflammatory factors and the apoptosis of hippocampal neurons. Its mechanism may be related to the inhibition of the Wnt/b-catenin signaling pathway.

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Depresión/metabolismo , MicroARNs/biosíntesis , Vía de Señalización Wnt/fisiología , beta Catenina/metabolismo , Animales , Antidepresivos de Segunda Generación/farmacología , Antidepresivos de Segunda Generación/uso terapéutico , Depresión/tratamiento farmacológico , Depresión/psicología , Fluoxetina/farmacología , Fluoxetina/uso terapéutico , Hipocampo/efectos de los fármacos , Hipocampo/metabolismo , Masculino , Ratones , Ratones Endogámicos C57BL , Distribución Aleatoria , Estrés Psicológico/tratamiento farmacológico , Estrés Psicológico/metabolismo , Estrés Psicológico/psicología , Vía de Señalización Wnt/efectos de los fármacos , beta Catenina/antagonistas & inhibidores

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OBJECTIVE: Nasopharyngeal carcinoma (NPC) is one of the most ordinary malignant tumors. Recent studies have revealed that circular RNAs play an important role in the progression of tumorigenesis. This study aims to identify how circular RNA_LARP4 functions in the progression of NPC. PATIENTS AND METHODS: We performed Real Time quantitative-Polymerase Chain Reaction (RT-qPCR) in 58 paired NPC patients' tissue samples and cell lines to detect circular RNA_LARP4 expression. The function of circular RNA_LARP4 in the NPC proliferation was identified by performing proliferation assay and colony formation assay. Moreover, the function of circular RNA_LARP4 in NPC metastasis was measured by performing scratch wound assay and transwell assay in vitro. Furthermore, the underlying mechanism was explored through Western blot assay and RT-qPCR. RESULTS: Circular RNA_LARP4 expression was significantly lower in NPC tissues compared to that in adjacent samples. Cell proliferation of NPC was inhibited after overexpression of circular RNA_LARP4 in vitro. Cell migration and invasion of NPC was inhibited after overexpression of circular RNA_LARP4 in vitro. Furthermore, the results of further experiments revealed that Rho-associated kinase 1 (ROCK1) was downregulated via overexpression of circular RNA_LARP4 and was also a direct target of circular RNA_LARP4 in NPC. CONCLUSIONS: This study suggests that circular RNA_LARP4 inhibits NPC cell proliferation and metastasis via targeting ROCK1 in vitro.

Asunto(s)

Carcinoma Nasofaríngeo/genética , Neoplasias Nasofaríngeas/genética , ARN Circular/genética , Quinasas Asociadas a rho/genética , Quinasas Asociadas a rho/metabolismo , Línea Celular Tumoral , Movimiento Celular , Proliferación Celular , Regulación hacia Abajo , Regulación Neoplásica de la Expresión Génica , Humanos , Carcinoma Nasofaríngeo/metabolismo , Neoplasias Nasofaríngeas/metabolismo , Invasividad Neoplásica , Metástasis de la Neoplasia

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OBJECTIVE: To investigate the effects of hyperbaric oxygen preconditioning (HBO-PC) on neuronal apoptosis, Ca2+ concentration, and Caspases expression after spinal cord injury (SCI) in rats. MATERIALS AND METHODS: A total of 36 rats were randomly divided into control group (CON group), hyperbaric oxygen preconditioning group (HBO-PC group) and spinal cord injury group (SCI group), with 12 rats in each group. Rats in group HBO-PC were given HBO-PC intervention before modeling. SCI model was established by modified Allen method in group HBO-PC and group SCI. Basso-Beattie-Bresnahan (BBB) locomotor rating scale and motor evoked potential (MEP) examination were used to assess the neurological function. The expression of apoptosis gene caspase (3, 7, 8, 12) mRNA was detected by reverse transcription-polymerase chain reaction (RT-PCR). The concentration of Ca2+ in spinal cord tissue of each group was detected. RESULTS: CON group, HBO-PC group, and SCI group were gradually diminishing in BBB score and potential value and amplitude of MEP, respectively. The differences between groups were statistically significant (p<0.05). The expressions of Caspase-3 and 7, 8 and 12 mRNA in SCI group were significantly higher than those in CON group and HBO-PC group, respectively (p<0.05). There was no significant difference between CON group and HBO-PC group (p>0.05). The concentrations of Ca2+ in the CON group, HBO-PC group and SCI group were gradually increased; differences between groups were statistically significant (p<0.05). CONCLUSIONS: HBO-PC can reduce the loss of motor function of SCI rats, which may inhibit the activation of endoplasmic reticulum pathway of neural apoptosis, and reduce the calcium overload through inhibiting the expressions of pro-apoptotic proteins (Caspase-3/7/8/12), thus reducing the cell apoptosis and protecting neurons.

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Apoptosis , Calcio/metabolismo , Caspasas/biosíntesis , Oxigenoterapia Hiperbárica , Neuronas/patología , Traumatismos de la Médula Espinal/metabolismo , Traumatismos de la Médula Espinal/patología , Animales , Potenciales Evocados Motores/fisiología , Femenino , Locomoción/fisiología , Masculino , Ratas , Traumatismos de la Médula Espinal/enzimología

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No disponible

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Humanos , Femenino , Adulto , Meningitis Aséptica/inducido químicamente , Meningitis Aséptica/complicaciones , Adalimumab/efectos adversos , Factor de Necrosis Tumoral alfa/análisis , Adalimumab/administración & dosificación , Psoriasis/tratamiento farmacológico , Tratamiento Biológico/efectos adversos

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Fusarium species are common plant pathogens present in the environment but can cause invasive infections in immunocompromised patients, especially those with haematologic malignancies and bone marrow transplant recipients1. Tissue and blood cultures are especially important as they offer a high diagnostic yield in invasive fusariosis2-3. Amphotericin B has been used as the mainstay of treatment4 although resistant rates are high, especially in Fusarium solani species5. The treatment outcome is also closely related to rate of recovery of neutropenia

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Disabling pansclerotic morphoea of childhood is a subset of localized scleroderma. It is a rare disease in both the adult and paediatric population. E t i o l ogical factors are unknown although autoimmune, infectious, genetic and environmental factors have been postulated. Sclerotic plaques predominantly affect the scalp, face, trunk and extensor surfaces of limbs, leaving fingertips and toes uninvo l ved. The absence of Raynaud’s phenomenon, dysphagia, visceral involvement and certain laboratory derangements diff e r e n t i a t e systemic sclerosis and disabling pansclerotic morphoea of childhood. Diagnosis can be supported by histology. There are seve r a l management options including topical, systemic and phototherapy.

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Churg-Strauss syndrome is a granulomatous smallvessel vasculitis in which multiple organ systems can be involved. It is often diagnosed late and physicians need to be vigilant and keep this uncommon diagnosis in mind. The appearance of visible cutaneous features is often the key to diagnosis and skin biopsy is confirmatory. Early recognition and aggressive therapy is required to prevent end-organ complications and mortality.

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AIMS: We aimed to investigate the sources of estrogen receptor alpha (ERalpha), estrogen receptor beta (ERbeta) and estimate the value of both ER subtypes in gastric adenocarcinoma and analyze the possible relationship of prothymosin alpha (ProTalpha) to ERs. METHODS: ERs at the mRNA and protein levels in matched advanced gastric adenocarcinomas and surrounding non-cancerous tissues were examined by using reverse transcription-polymerase chain reaction and immunohistochemical (IHC) methods. Cell proliferation related protein ProTalpha was also detected in IHC. The immunoreactive signal, corresponding to the proteins expression level, was quantitatively analyzed. RESULTS: Both ERalpha and ERbeta mRNAs were detected in most of the cancer and matched normal tissues analyzed. At the protein level, the percentage of ERalpha and ERbeta positive cases changed. ERalpha immunoreactivity was only detected in poorly differentiated adenocarcinoma and ERalpha positive expression correlated with depth of invasion of the tumors. Compared with non-cancerous tissues, gastric tumors showed decreased ERbeta expression and lost ERbeta. Altered ERbeta in gastric adenocarcinoma correlated with decreased differentiation. And the tumors involved lymph node metastasis showed significantly lower expression level of ERbeta. ProTalpha in ERbeta-positive tumors showed higher expression than that in lost ERbeta tumors. CONCLUSIONS: Altered expression of ERalpha and ERbeta in tumors compared with corresponding normal gastric tissues was more common in poorly differentiated adenocarcinomas and related to malignant properties, such as lymph node metastasis. Decreased ERbeta and increased ProTalpha expression in advanced gastric adenocarcinoma indicated that ERbeta may play an anti-proliferation role which is opposed to the role of ProTalpha in gastric epithelium.

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Adenocarcinoma , Receptor alfa de Estrógeno/genética , Receptor beta de Estrógeno/genética , Regulación Neoplásica de la Expresión Génica , Precursores de Proteínas/genética , ARN Neoplásico/genética , Neoplasias Gástricas , Timosina/análogos & derivados , Adenocarcinoma/genética , Adenocarcinoma/metabolismo , Adenocarcinoma/patología , Adulto , Anciano , Anciano de 80 o más Años , Biomarcadores de Tumor/biosíntesis , Biomarcadores de Tumor/genética , Diferenciación Celular , Receptor alfa de Estrógeno/biosíntesis , Receptor beta de Estrógeno/biosíntesis , Femenino , Humanos , Inmunohistoquímica , Masculino , Persona de Mediana Edad , Estadificación de Neoplasias , Pronóstico , Precursores de Proteínas/biosíntesis , Reacción en Cadena de la Polimerasa de Transcriptasa Inversa , Índice de Severidad de la Enfermedad , Neoplasias Gástricas/genética , Neoplasias Gástricas/metabolismo , Neoplasias Gástricas/patología , Timosina/biosíntesis , Timosina/genética